Myc is a transcription factor and key cell growth regulator that is frequently deregulated in human malignancy, notably Burkitt's and T cell lymphomas, where myc genes suffer chromosomal translocation. In colon and lung carcinomas, myc genes are amplified [M. D. Cole, Ann. Rev. Genet., 20:361-384 (1986)]. Paradoxically, under certain conditions myc can induce apoptosis [D. S. Askew et al, Oncogene, 6:1915-1922 (1991); G. I. Evan et al, Cell, 69:119-128 (1992)], a phenotype consistent with its original identification (and naming) as a retroviral gene that induces myelocytomatosis (myeloid cell death) as well as tumorigenesis [D. Sheiness et al, J. Virol., 28:600-610 (1978)]. Loss or suppression of apoptosis is an important step in the malignant conversion of human tumors containing deregulated myc oncogenes, including, prominently, prostate carcinoma [T. G. Strohmeyer et al, J. Urol., 151:1479-1497 (1994)].
There remains a need in the art for compositions and methods of regulating a deregulated Myc protein and/or diagnosing the occurrence of such deregulation.